Linking the removal of enrofloxacin to the extracellular polymers of microalgae in water bodies: A case study focusing on the shifts in microbial communities.

Microalgae can promote antibiotic removal, which has attracted growing attention. However, its synergistic removal performance with bacteria in antibiotic pollutants is still poorly understood. In this study, firstly, we selected two green algae (Dictyosphaerium sp. and Chlorella sp.) and exposed them to Enrofloxacin (ENR) to observe their extracellular polysaccharides (EPS) concentration dynamic and the removal of antibiotics. Secondly, EPS was extracted and added to in situ lake water (no algae) to investigate its combined effect with bacteria. The results indicate that both Dictyosphaerium sp. and Chlorella sp. exhibited high tolerance to ENR stress. When the biomass of microalgae was low, ENR could significantly stimulate algae to produce EPS. The removal rates of Dictyosphaerium sp. and Chlorella sp. were 15.8% and 10.5%, respectively. The addition of EPS can both alter the microbial community structure in the lake water and promote the removal of ENR. The LEfSe analysis showed that there were significant differences in the microbial marker taxa, which promoted the increase of special functional bacteria for decomposing ENR, between the EPS-added group and the control group. The EPS of Dictyosphaerium sp. increased the abundance of Moraxellaceae and Spirosomaceae, while the EPS of Chlorella sp. increased the abundance of Sphingomonadaceae and Microbacteriaceae. Under the synergistic effect, Chlorella sp. achieved a maximum removal rate of 24.2%, while Dictyosphaerium sp. achieved a maximum removal rate of 28.9%. Our study provides new insights into the removal performance and mechanism of antibiotics by freshwater microalgae in water bodies and contribute to the development of more effective water treatment strategies.

Interfacial polymerization mechanisms assisted flame retardancy process of low-flammable electrolytes on lithium anode.

Thermal runaway is a hazardous risk, occurring more readily in high-energy-density lithium-ion batteries (LIBs), which leads to a rapid temperature rise and even combustion or explosion when using flammable electrolyte systems. Flame retardants (FRs), such as trimethyl phosphate (TMPa) and triethyl phosphate (TEP), are commonly utilized due to their effective flame suppression, low toxicity, and excellent thermal stability. However, the lack of in-depth understanding of the flame retardancy mechanism and solid electrolyte interphase (SEI) formation process has made the development of functional electrolytes difficult at present. In this study, we clarified the flame retardancy and interfacial reaction mechanisms of low-flammable TMPa localized high-concentration electrolytes (LHCE) using hybrid ab initio and reactive force field (HAIR) schemes. Long-term HAIR simulation reveals that phosphorous radicals produced by the decomposition of TMPa capture carbon radicals, encouraging their polymerization into low-flammable oligomers, while fluorine-containing solvents in the electrolyte capture hydrogen radicals and produce nonflammable hydrofluoric acid (HF). This synergistic flame retardancy mechanism provides essential atomic-level insights for the rational design of high-safety electrolytes in the future.

Prognostic risk factor analysis and nomogram construction for primary liver cancer in elderly patients based on SEER database.

OBJECTIVE: To evaluate the risk factors and construct a nomogram model for the prognosis of primary liver cancer in the elderly based on the data from the US SEER database. METHODS: The latest data of patients with primary liver cancer were extracted from the SEER database using SEER*STAT software, and the required variables were included. The data were screened and then divided into a training cohort and a validation cohort. A nomogram model was constructed by screening the variables through univariate and multivariate Cox analysis. The C-Index, ROC and calibration curves were used for model evaluation. RESULTS: A total of 10 824 eligible cases from 2004 to 2017 were extracted, among which, 7757 cases were included in the training cohort and 3247 in the validation cohort. The C-Index of the model was 0.747 (in the training cohort) and 0.773 (in the validation cohort). The 3-year area under the curve (AUCs) of the training and the validation cohorts were 0.760 and 0.750, and the 5-year AUCs of the two cohorts were 0.761 and 0.748. The calibration curves showed an ideal calibration of the constructed model. CONCLUSIONS: The nomogram model constructed followed by Cox regression analysis showed moderate calibration and discrimination property, and can provide reference to a certain extent for furture clinical application of primary liver cancer in the elderly.

Prevalence of frailty and prediction of mortality in Chinese cancer patients using a frailty index-based clinical algorithm-A multicentre study.

PURPOSE: To investigate the frailty status in Chinese cancer patients through establishing a novel prediction algorithm. METHODS: The percentage of frailty in various age groups, locations, and tumor types in Chinese cancer patients was investigated. The prediction capacity of frailty on mortality of Chinese cancer patients was analysed by the frailty index composing of routine laboratory data (FI-LAB) accessible from a blood test and calculated as the ratio of abnormal factors to 22 total variables. The establishment of a novel algorithm, MCP (mortality of cancer patients), to predict the 5-year mortality in Chinese cancer patients was accomplished and the algorithm's prediction capacity was tested in the training and validation sets using receiver operating characteristic (ROC) analysis. RESULTS: We found that the risk of death in cancer patients can be successfully identified through FI-LAB. The univariable and multivariable Cox regression were used to evaluate the effect of frailty on death. In the 5-year follow-up, 20.6% of the 2959 participants (age = 55.8 ± 11.7 years; 43.5% female) died, while the mean FI-LAB score in baseline was 0.23 (standard deviation = 0.13; range = 0-0.73). Frailty (after adjusting for gender, age, and other confounders) directly correlated with an increased risk of death, hazard ratio of 12.67 (95% confidence interval [CI]: 7.19, 22.31), compared to those without frailty. In addition, the MCP algorithm (MCP) = 3.678 × FI-LAB + 1.575 × sex + 1.779 × first tumor node metastasis staging, presented an area under the ROC (AUC) of 0.691 (95% CI: 0.656-0.726) and 0.648 (95% CI: 0.613-0.684) in the training and validation sets, respectively. CONCLUSION: Frailty as defined by FI-LAB was common and indicated a significant death risk in cancer patients. Our novel developed algorithm MCP had a passable prediction capacity on 5-year MCP.

Correlation between lncRNA SNHG16 gene polymorphism and its interaction with environmental factors and susceptibility to colorectal cancer.

OBJECTIVE: To study the relationship between long-chain non-coding RNA small nucleolar RNA host gene 16 (lncRNA SNHG16) polymorphisms and its interaction with environmental factors and susceptibility to colorectal cancer (CRC). METHODS: Sanger sequencing was used to analyze genotypes of lncRNA SNHG16 gene rs7353, rs8038, and rs15278 sites. Multifactor dimensionality reduction was used to analyze interactions between lncRNA SNHG16 gene rs7353, rs8038, rs15278 sites, and environmental factors. Haploview 4.1 software was used to analyze linkage disequilibrium of lncRNA SNHG16 gene rs7353, rs8038, and rs15278 sites. Quantitative real-time polymerase chain reaction was used to analyze plasma lncRNA SNHG16 levels of CRC patients and control subjects. RESULTS: Variation of the lncRNA SNHG16 gene rs7353 site A>G variation was associated with decreased CRC susceptibility (Odds ratio [OR] = 0.50, 95% confidence interval [CI]: 0.40-0.62, P < .01). The rs8038 site G>A and rs15278 site A>G variation were associated with increased CRC susceptibility (OR = 1.87, 95% CI: 1.47-2.36, P < .01). The rs15278 site G>A variation was associated with increased CRC susceptibility (OR = 2.24, 95% CI: 1.61-3.11, P < .01). Interaction combinations featuring age, rs7353, rs8038, and rs15278 single nucleotide polymorphism are 13.53 times more susceptible to CRC than other interactions (95% CI: 9.43-19.41, P < .01). The rs15278, rs8038, and rs7353 site AGA haplotypes were significantly associated with a decreased CRC risk (OR = 0.65, 95% CI: 0.48-0.88, P = .01), AAG haplotypes were significantly associated with an increased CRC risk (OR = 2.00, 95% CI: 1.27-3.17, P < .01). High lncRNA SNHG16 expression was associated with tumor progression in CRC patients (χ = 8.85, P = .03). The rs7353 site A>G variation caused a significant decrease in plasma lncRNA SNHG16 level (P < .01), while the rs8038 site G>A variation and rs15278 site A>G variation resulted in increased plasma lncRNA SNHG16 levels. CONCLUSION: Polymorphisms of lncRNA SNHG16 gene rs7353, rs8038, rs15278 loci and their interaction with age are significantly associated with CRC susceptibility.

Adipose-derived mesenchymal stem cells alleviate TNBS-induced colitis in rats by influencing intestinal epithelial cell regeneration, Wnt signaling, and T cell immunity.

BACKGROUND: Conventional Crohn's disease (CD) treatments are supportive rather than curative and have serious side effects. Adipose-derived mesenchymal stem cells (ADSCs) have been gradually applied to treat various diseases. The therapeutic effect and underlying mechanism of ADSCs on CD are still not clear. AIM: To investigate the effect of ADSC administration on CD and explore the potential mechanisms. METHODS: Wistar rats were administered with 2,4,6-trinitrobenzene sulfonic acid (TNBS) to establish a rat model of CD, followed by tail injections of green fluorescent protein (GFP)-modified ADSCs. Flow cytometry, qRT-PCR, and Western blot were used to detect changes in the Wnt signaling pathway, T cell subtypes, and their related cytokines. RESULTS: The isolated cells showed the characteristics of ADSCs, including spindle-shaped morphology, high expression of CD29, CD44, and CD90, low expression of CD34 and CD45, and osteogenic/adipogenic ability. ADSC therapy markedly reduced disease activity index and ameliorated colitis severity in the TNBS-induced rat model of CD. Furthermore, serum anti-sacchromyces cerevisiae antibody and p-anti-neutrophil cytoplasmic antibody levels were significantly reduced in ADSC-treated rats. Mechanistically, the GFP-ADSCs were colocalized with intestinal epithelial cells (IECs) in the CD rat model. GFP-ADSC delivery significantly antagonized TNBS-induced increased canonical Wnt pathway expression, decreased noncanonical Wnt signaling pathway expression, and increased apoptosis rates and protein level of cleaved caspase-3 in rats. In addition, ADSCs attenuated TNBS-induced abnormal inflammatory cytokine production, disturbed T cell subtypes, and their related markers in rats. CONCLUSION: Successfully isolated ADSCs show therapeutic effects in CD by regulating IEC proliferation, the Wnt signaling pathway, and T cell immunity.